Six New Studies Illuminate Causes and Comorbidities in Migraine

Hans-Christoph Diener, MD, PhD


August 26, 2016

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Dear colleagues, I'm Dr Christoph Diener, a neurologist from the University Hospital of Essen in Germany. Usually I report one important study from the past month. But this July I found six extremely important publications on the topic of migraine, which I will report here.

It starts with a paper in Nature Genetics[1] from Harvard Medical School. The investigators did a whole genome sequence in 59,674 patients with migraine and 316,078 controls. They identified 38 new susceptibility loci for migraine, which code for vascular and smooth muscle tissue. This would again indicate that the endothelium plays a very important role in the pathophysiology of migraine.

The next publication, by Kurth and colleagues from the Nurses' Health Study 2, was published in the British Medical Journal.[2] This is a joint venture between Harvard Medical School and the Charité in Berlin. They analyzed data from 115,541 women (age range, 25-42 years) who were then followed for 20 years. In participating nurses who suffered from migraine, the hazard ratio was 1.5 for a major vascular event and 1.62 for stroke. This again indicates that there is a very small absolute increase in the risk for stroke in female patients with migraine. In such females, I think it's a good idea to identify vascular risk factors and controls, in particular high blood pressure and smoking.

The third study is again from Harvard Medical School and was published in the journal Brain.[3] We all know that migraine patients suffer from photophobia. The 69 patients in this study were exposed to different colors during photophobia. The researchers found that green light exacerbates headache. This would indicate that there are cone-driven retinal pathways, which really contribute to photophobia and migraine.

The next paper was also published in Brain[4] and comes from researchers in Hamburg. The investigators put a female patient into an MRI scan and evoked pain responses by stimulating the trigeminal nerve. They did this every day for 30 consecutive days, and the patient suffered three spontaneous migraine attacks. What they found was that, obviously, prior to and during a migraine attack, there are several brain structures which become active. One is the hypothalamus prior to the attack, and then during the attack, the trigeminal nucleus, and the migraine generator in the dorsal pons.

The fifth study, also published in Brain,[5] is from Copenhagen. The researchers looked at whether patients with migraine with aura have a higher risk for white matter lesions and silent strokes. They had 172 cases with migraine with aura, 139 controls, and then 34 twin pairs in which one of the twins had migraine with aura and the other had no migraine. They were not able to identify a higher risk for silent strokes or white matter lesions in patients with migraine.

The final publication, in the European Heart Journal,[6] is a randomized trial in 107 patients with migraine with aura and patent foramen ovale (PFO). Half of these patients received an occlusion of the PFO with an Amplatzer® device [St. Jude Medical; St. Paul, Minnesota]. After 1 year, there was no difference in the frequency of migraine attacks between patients in whom the PFO was closed and patients in whom the PFO was left open. I have to mention that all of these patients received clopidogrel for 3 months and aspirin for 6 months, which has a certain migraine-preventive activity.

So, lots of new, very exciting information on migraine has appeared, some of which may have immediate consequences for the treatment of our patients with migraine.

Ladies and gentlemen, I am Dr Christoph Diener, a headache specialist from the University Hospital in Essen in Germany. Thank you for listening.


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